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An initial biphasic model of the human heart aimed at computational investigation of rheumatic heart disease
Published in Alphose Zingoni, Insights and Innovations in Structural Engineering, Mechanics and Computation, 2016
G. Hopkins, S. Skatulla, L. Moj, T. Ricken, N. Ntusi, E. Meintjes
Effective treatment of this condition requires a sound understanding of the underlying failure mechanisms involved. However, due to improved socio-economic conditions, infection rates of ARF are extremely low in developed countries, and as a result research capacity in this field is scarce (Sliwa & Zilla 2012, Essop & Nkomo 2005). In terms of heart valve replacement therapy, progress has been made allowing the heart to regenerate. However, in such therapy the main focus has been on the infectious and inflammatory processes of ARF and less so on the subsequent proliferative responses (growth and remodelling) of the myocardium. In this sense, research aiming specifically at the tertiary prevention and treatment of RHD remains inadequate. The development of effective treatment strategies requires an understanding of how changes to proliferative mechanisms caused by medication impact on the adverse ventricular remodelling process and improve the overall pumping capacity of the heart. To this end, unobtrusive research tools are required to be developed to further investigate the progression of the disease.
Development of a three dimensional (3D) knitted scaffold for myocardial tissue engineering. Part II: biological performance of the knitted scaffolds
Published in The Journal of The Textile Institute, 2025
Derya Haroglu, Ahmet Eken, Zeynep Burçin Gönen, Dilek Bahar
The World Health Organization (WHO) reported that more than 9 million people died from coronary artery disease (CAD) throughout the World in 2016, accounting for approximately 53% of all deaths due to cardiovascular diseases (CVDs) (World Health Organization, 2017). CVD has been the primary cause of death globally for more than two decades (World Health Organization, 2017). Myocardial infarction (MI), also called as heart attack, is a significant health problem for patients with CAD. MI can be characterized as cardiac cell death due to blocking of oxygen and nutrients supply from the blood to a region of the heart muscle (or myocardium) (Thygesen et al., 2007, 2012). This can be caused by the abrupt 100% occlusion of the coronary arteries supplying blood to the related region of the heart (Thygesen et al., 2007, 2012). Up to one billion cardiomyocytes (CMs), the contractile cardiac cells, mostly in the human left ventricule, might be lost irreversibly within the first hours of acute MI (Giraud et al., 2007; Laflamme & Murry, 2011). Since CMs have limited regenerative ability, less than or equal to 1% per year, dead CMs are replaced by a non-contractile scar in the infarct-related region of the heart within months in patients who survive the acute MI (Pfeffer & Braunwald, 1990; Tzahor & Poss, 2017). The loss of contractile tissue induces ventricular remodeling, dilatation, and thinning of the injured ventricle, and impairs the pumping function of the heart, which could cause further cardiomyocyte loss, resulting in heart failure, and ultimately death (Pfeffer & Braunwald, 1990; Zhu et al., 2019).